In recent years, improved surgical technique and myocardial preservation during procedures involving cardiopulmonary bypass (CPB) have significantly reduced perioperative cardiac, and overall, morbidity and mortality. However, despite major advances in myocardial protection during CPB, patients undergoing CPB and heart surgery continue to sustain significant rates of postoperative alterations in neurologic and neuropsychologic function. These changes range from subtle neurologic deficits (e.g., patients "do not seem to be themselves"), to overt sensorimotor deficits (e.g., stroke), to post-operative brain death. For example, investigators--using state of the art testing techniques--have identified neurologic deficits (i.e., fatal cerebral injury, stroke, impaired level of consciousness, and seizures) in 1-6% of patients following CPB. See Mills SA: Cerebral injury and cardiac operations. Ann Thorac Surg 1993; 56:S86-91, which article is incorporated herein by reference. They also noted neuropsychologic deficits (i.e., cognitive changes quantified with tests of memory, learning, and speed of visual-motor response) in 60-80% and 20-40% of patients at 1 wk and 8 wk following cardiac surgery, respectively. Other investigators have reported that neurologic injury is the second most frequent cause of death (i.e., accounting for approximately 20% of CPB-related deaths) following CPB. See Nussmeier NA, Arlund C, Slogoff S: Neuropsychiatric complications after cardiopulmonary bypass: Cerebral protection by a barbiturate. Anesthesiology 1986; 64:165-170, which article is incorporated herein by reference. Thus, there is a need for a method to simultaneously optimize both cardiac and neurologic outcome following CPB and, in particular, following cardiac surgery.
It is widely believed that neurologic injury accompanying CPB is of an ischemic origin. Specifically, it is believed that during CPB low flow states and showers of air and particulate emboli washed into the cerebral circulation produce an ischemic insult that is primarily of a multifocal ischemic pattern. There is ample experimental evidence--predominantly using transcranial Doppler (TCD)-facilitated assessment of the cerebral circulation--to support this theory. For example, Mills described mean embolic counts (i.e., the mean number of discrete embolic events detected) of 50 and 207 in coronary artery bypass grafting (CABG) patients having an aortic plaque thickness measuring &lt;5 mm and &gt;5 mm, respectively. Albin et al. (see Albin MS, Hantler GB, Mitzel H: Aeric microemboli and the transcranial Doppler (TCD): Episodic frequency and timing in 62 cases of open heart surgery. Anesthesiology 1991; 75:A53, which article is incorporated herein by reference.) reported a mean embolic count of approximately 360 at the completion of CPB in patients having "open" heart surgery (e.g., as occurs with valve repair or replacement). In contrast, patients having "closed" heart surgery (e.g., as occurs with CABG) experienced half that number of air emboli at the same study interval. These observations correlate well with a more than two-fold greater incidence of postoperative neuropsychiatric deficits in "open" versus "closed" heart surgery patients. See Slogoff S, Girgis KZ, Keats AS: Etiologic factors in neuropsychiatric complications associated with cardiopulmonary bypass. Anesth Analg 1982; 61:903-911, which article is incorporated herein by reference. Albin et al. also reported previously unsuspected episodes of no cerebral blood flow (CBF) ranging in duration from 4 s to longer than 2 min during otherwise apparently uneventful CPB. The latter events, while insufficient to cause irreversible brain injury alone, may be sufficient to exacerbate injury resulting from air and particulate emboli.
It is also well known that alterations in temperature can affect the brain's ability to survive an ischemic insult. This phenomenon has been demonstrated repeatedly in humans subjected to profound hypothermia and circulatory arrest to facilitate the surgical repair of complex cardiac or cerebrovascular anomalies. When temperature is reduced to 17-20.degree. C., the human brain can tolerate approximately one hour of circulatory arrest without sustaining permanent injury. This dramatic evidence of cerebral protection is believed to be mechanistically related to large reductions in the cerebral metabolic rate of oxygen consumption (CMRO.sub.2) that occur during profound hypothermia. It has also been demonstrated that mild alterations in brain temperature can have a significant effect on functional outcome and histopathology following cerebral ischemia. In these studies, improvement in outcome was reported with mild hypothermia and worsened with mild hyperthermia.
The most dramatic examples of modulation of ischemic brain injury by small alterations in brain temperature have been reported by Wass et al. (See Wass CT, Lanier WL, Hofer RE, Scheithauer BW, Andrews AF: Temperature changes of .gtoreq.1.degree. C. alter functional neurologic outcome and histopathology in a canine model of complete cerebral ischemia. Anesthesiology 1995; 83:325-335, which article is incorporated herein by reference) and Warner et al. (See Warner DS, McFarlane C, Todd MM, Ludwig P, McAllister AM: Sevoflurane and halothane reduce focal ischemic brain damage in the rat: Possible influence in thermoregulation. Anesthesiology 1996; 79:985-992, which article is incorporated herein by reference). The former investigators discovered that temperature changes of either 1 or 2.degree. C. altered functional and histologic outcome in a canine model of complete cerebral ischemia. The latter authors discovered that a change in brain temperature of 1.2.degree. C. altered functional and histologic outcome in a rat model of focal cerebral ischemia.
Although the exact physiologic basis by which small temperature changes produce significant alterations in post-ischemic neurologic outcome is not clear, it is apparent such changes can have a significant effect on functional outcome and histopathology following cerebral ischemia.
One technique known in the prior art for attempting to achieve cerebral cooling during major vascular or complex cardiac surgery has been attempted by packing the patient's head in ice. However, this technique suffers from various drawbacks, including posing a serious risk of frostbite injury to the patient.